Preceding infections, immune factors, and outcome in Guillain-Barre syndrome

Citation
Rdm. Hadden et al., Preceding infections, immune factors, and outcome in Guillain-Barre syndrome, NEUROLOGY, 56(6), 2001, pp. 758-765
Citations number
43
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
56
Issue
6
Year of publication
2001
Pages
758 - 765
Database
ISI
SICI code
0028-3878(20010327)56:6<758:PIIFAO>2.0.ZU;2-8
Abstract
Objective: To test the hypothesis that different preceding infections influ ence the neurophysiologic classification and clinical features of Guillain- Barre syndrome (GBS). Methods: We tested pretreatment sera, 7 +/- 3 (mean /- SD) days from onset, from 229 patients with GBS in a multicenter trial o f plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurop hysiologic and clinical features. Results: Recent infection by Campylobacte r jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Ep stein-Barr virus in four (2%). Patients with C, jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy o r inexcitable nerves, antiganglioside GM, antibodies, pure motor GBS, lower CSF protein, and worse outcome, Patients with cytomegalovirus infection we re younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble in tercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion m olecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R). Concentrations of sICAM-1 and soluble tumor necrosis fac tor receptor were higher in patients with inexcitable nerves than those wit h demyelinating neurophysiology. Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, ine xcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentrat ion and absence of immunoglobulin (Ig) M antiganglioside GM, antibodies. Co nclusions: Subtypes of GBS defined by preceding infections were only approx imately associated with different patterns of clinical, neurophysiologic, a nd immunologic features. A single infectious agent caused more than one typ e of pathology in GBS, implying interaction with additional host factors. M ost patients had no identified infection.